Hermán F, Malomvölgyi B, Hadházy P, Magyar K
Department of Pharmacodynamics, Semmelweis University of Medicine, Budapest, Hungary.
Biomed Biochim Acta. 1988;47(10-11):S90-3.
The arterial blood of anaesthetized heparin-treated beagle dogs was directed through a 30/um diameter pore size screen by a roller pump at a constant rate. As a result, the pressure proximal to the filter continuously increased. The filtration pressure stabilizing concentration of prostacyclin (infused proximal to the filter) was determined. BM 13.177 -similar to PGI2- was able to slow down and stop the increase of filtration pressure (final conc.: 1-10/uM). In addition it could reverse the filter occlusion process. The lowest concentration of BM 13.177 (0.1-1/uM) did not affect significantly the filter occlusion rate, but it markedly enhanced the antiaggregatory effect of PGI2 when these drugs were administered simultaneously. In summary, we can conclude that 1) generation of thromboxane and endoperoxide plays a key role in the mechanism of the spontaneous platelet aggregation on the filter; 2) BM 13.177 significantly potentiates the antiaggregatory effect of PGI2 in vivo.
通过滚轴泵以恒定速率将麻醉的、经肝素处理的比格犬的动脉血引导通过孔径为30微米的滤网。结果，滤网近端的压力持续升高。测定了前列环素（在滤网近端注入）的过滤压力稳定浓度。BM 13.177（类似于PGI2）能够减缓并阻止过滤压力的升高（最终浓度：1 - 10微摩尔）。此外，它还能逆转滤网堵塞过程。BM 13.177的最低浓度（0.1 - 1微摩尔）对滤网堵塞速率没有显著影响，但当这些药物同时给药时，它能显著增强PGI2的抗聚集作用。总之，我们可以得出以下结论：1）血栓素和内过氧化物的生成在滤网上自发血小板聚集的机制中起关键作用；2）BM 13.177在体内显著增强PGI2的抗聚集作用。
